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[家兔吗啡镇痛中伏隔核至杏仁核的神经通路]

[The neural pathway from nucleus accumbens to amygdala in morphine analgesia of the rabbit].

作者信息

Yu L C, Han J S

机构信息

Department of Physiology, Beijing Medical University.

出版信息

Sheng Li Xue Bao. 1990 Jun;42(3):277-83.

PMID:2082473
Abstract

The purpose of this study was to explore possible neural connections between the nucleus accumbens and amygdala involved in analgesia. The latency of the escape response elicited by radiant heat applied on snout of the rabbit was taken as an index for nociception. It was found that: (1) the analgesic effect elicited by intra-accumbens injection of morphine was attenuated dose-dependently by intra-amygdala administration of opioid antagonist naloxone, or antisera against met-enkephalin (ME) or beta-endorphin (beta-EP), suggesting the involvement of ME and beta-EP in the accumbens-amygdala connection; (2) the analgesia produced by intra-amygdaloid injection of morphine was not affected by naloxone administered to nucleus accumbens, suggesting a one-way connection between the two nuclei; (3) the analgesia of intra-accumbens injection of morphine was significantly attenuated by muscimol, the GABA receptor agonist, and enhanced by bicuculline methochloride, the GABA receptor antagonist injected into the same site where morphine was administered. The results suggest that the analgesic effect of morphine administered to the nucleus accumbens is mediated by the suppression of the GABAergic inhibitory neurons located within the nucleus.

摘要

本研究的目的是探索伏隔核与杏仁核之间可能参与镇痛的神经连接。将辐射热作用于兔鼻引起的逃避反应潜伏期作为伤害感受的指标。结果发现:(1) 杏仁核内注射阿片类拮抗剂纳洛酮、甲硫氨酸脑啡肽(ME)或β-内啡肽(β-EP)的抗血清,可剂量依赖性地减弱伏隔核内注射吗啡引起的镇痛作用,提示ME和β-EP参与伏隔核-杏仁核连接;(2) 杏仁核内注射吗啡产生的镇痛作用不受伏隔核注射纳洛酮的影响,提示两核之间存在单向连接;(3) 伏隔核内注射吗啡的镇痛作用被GABA受体激动剂蝇蕈醇显著减弱,而被注入吗啡给药部位的GABA受体拮抗剂氯化荷包牡丹碱增强。结果表明,伏隔核注射吗啡的镇痛作用是通过抑制伏隔核内的GABA能抑制性神经元介导的。

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引用本文的文献

1
Altered nucleus accumbens circuitry mediates pain-induced antinociception in morphine-tolerant rats.伏隔核神经回路的改变介导了吗啡耐受大鼠的疼痛诱导性抗伤害感受。
J Neurosci. 2002 Aug 1;22(15):6773-80. doi: 10.1523/JNEUROSCI.22-15-06773.2002.